气道重塑是哮喘的关键特征，上皮-间质转化（EMT）被认为是成纤维细胞新的来源，能够促进气道重塑，但其机制尚不清楚。我们前期研究发现：DEK 和Six1以及Ezrin在哮喘模型小鼠肺组织上皮中高表达，将DEK沉默后Six1和Ezrin蛋白表达减少及气道重塑明显缓解；免疫双荧光显示Six1和Ezrin 共表达于16BHE细胞内。本课题假设DEK通过上调Six1/Ezrin信号通路诱导EMT促进哮喘气道重塑，并从分子、细胞和整体层面，拟通过蛋白表达分析和芯片检测技术以及免疫共沉淀和流式细胞等技术，探讨 DEK 基因和 Six1/Ezrin 信号通路间的基因表达调控关系；阐明DEK 通过上调Six1/Ezrin 信号通路引发 EMT 促进气道重塑的发展。本研究将证实 DEK通过Six1/Ezrin信号通路促进气道重塑的分子作用机制，为哮喘气道重塑进一步提供新的理论依据。

Airway remodeling is a key feature of asthma, and epithelial-mesenchymal transition (EMT) is considered a new source of fibroblasts that are able to promote airway remodeling, but the mechanism is unclear. Our previous studies found that DEK, Six1 and Ezrin were highly expressed in the epithelium of lung tissues of asthmatic mice models, and the expression of Six1 and Ezrin proteins were reduced and airway remodeling was significantly relieved after silencing DEK. Immuno-double fluorescence showed that Six1 and Ezrin were co-expressed in 16BHE cells. However, the relationship between DEK and the Six1/Ezrin signaling pathway and the effect on EMT have not been reported. In this study, we intend to investigate the gene expression regulation relationship between DEK gene and Six1/Ezrin signaling pathway using protein expression analysis and microarray detection techniques; and to elucidate that DEK triggers EMT through Six1/Ezrin signaling pathway leading to the evolution of airway remodeling from molecular, cellular and overall levels through co-immunoprecipitation and flow cytometry techniques.This study will confirm the molecular mechanism of DEK in promoting airway remodeling through Six1/Ezrin signaling pathway, providing a new molecular target and theoretical basis for clinical treatment of airway remodeling in asthma.